Evidence map›Paper›PMID 41050713›Full record

ArticleClinical, cosmetic and investigational dermatology2025

Interleukin-1 Receptor Antagonist as a Potential Mediator Linking Psoriasis and Non-Alcoholic Fatty Liver Disease: Insights From Mendelian Randomization and Experimental Evidence.

Ce Shuai, Szeman Cheung, Li Zhang, Han Cao, Yongyong Yuan, Qinyi Ge, Youcong Wang, Xia Li, Jie Zheng, Feng Xue

Abstract read
In one paragraph

Article in Clinical, cosmetic and investigational dermatology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors.

Ce Shuai *Department of Dermatology, Ruijin Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, People's Republic of China.
Szeman Cheung *Department of Dermatology, Ruijin Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, People's Republic of China.
Li ZhangDepartment of Dermatology, Ruijin Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, People's Republic of China.
Han CaoDepartment of Dermatology, Ruijin Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, People's Republic of China.
Yongyong YuanDepartment of Dermatology, Ruijin Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, People's Republic of China.
Qinyi GeDepartment of Dermatology, Ruijin Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, People's Republic of China.
Youcong WangDepartment of Dermatology, Ruijin Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, People's Republic of China.
Xia LiDepartment of Dermatology, Ruijin Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, People's Republic of China.
Jie ZhengDepartment of Dermatology, Ruijin Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, People's Republic of China.
Feng XueDepartment of Dermatology, Ruijin Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, People's Republic of China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Epidemiological studies have revealed a close association between psoriasis and non-alcoholic fatty liver disease (NAFLD), but the causal relationship and underlying mechanisms remain unclear. Materials and Methods: In this study, we used genome-wide association study (GWAS) data from the MRC Integrative Epidemiology Unit (MRC-IEU) to investigate the causal relationship between psoriasis and NAFLD, as well as potential mediators. Two-sample and two-step MR analyses were conducted, followed by bulk and single-cell transcriptomic analyses to validate our MR findings. In vivo validation was performed using Enzyme-Linked Immunosorbent Assay (Sample of patients (n=10)), immunohistochemistry, and liver bulk transcriptomic analysis. Results: The two-sample MR analysis revealed that genetically predicted psoriasis significantly increased the risk of NAFLD (OR = 1.07, 95% CI = 1.03-1.12, Conclusion: Our study demonstrates that genetically predicted psoriasis increases the risk of NAFLD, and plasma IL-1RA may serve as a potential mediator between psoriasis and NAFLD.

Indexed as

imiquimod-induced mouse modelmendelian randomizationnon-alcoholic fatty liver diseasepsoriasis

Identifiers

PMID41050713
PMCPMC12493115

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.